1. Field of the Invention
The present invention relates to dental instruments and, more particularly, to laser augmented periodontal scaling instruments (LAPSI). Such instruments are particularly applicable in the treatment of periodontal pockets and other periodontal disease.
2. Description of the Prior Art
The Periodontal Pocket and Periodontitis
A periodontal pocket is a gingival sulcus that has been pathologically deepened beyond three millimeters by an apical migration of the gingival attachment. This apical migration of the gingival attachment occurs because the supporting periodontal tissues have been compromised or destroyed and ultimately leads to the loosening of the tooth and eventual dental exfoliation if left unchecked and untreated. There are many clinical signs associated with the periodontal pocket, including thickened marginal gingiva, gingival bleeding, production of pus, tooth mobility, tooth migration, and pain. To locate and correctly diagnose a periodontal pocket, a comprehensive probing of the tooth must be done with a periodontal probe, and x-rays must be examined, to locate the depth of the pocket and extent of the destruction.
The etiology and pathogenesis of the periodontal pocket and hence periodontal disease is well understood. The main culprits are pathogenic bacteria that create a localized immune and inflammatory response to the microbial insult, mitigating massive and insidious local tissue destruction. These pathogenic bacteria can be found in the periodontal architecture of the soft tissue of the pocket, the exposed cementum, or dentin of the tooth. As inflammatory changes begin to occur in the connective tissues of the gingival sulcus (because of this bacterial insult), deleterious cellular exudate and microbial infiltration begin to degrade the gingival fibers connecting the tissue to the tooth (the periodontal ligament). As the collagen fibers of this attachment are broken down, the area is filled with inflammatory cells and edematous fluids. As this attachment tissue loses its cohesiveness, it detaches from the surface of the cementum and migrates apically forming the periodontal pocket. This progression will create an area around the tooth that cannot be adequately cleansed with local plaque removal techniques, will harbor large amounts of the causative pathogenic bacteria, and establish a continuous repeating process that once begun will ultimately lead to periodontal disease and tooth loss.
The periodontal pocket is generally considered to be a chronic inflammatory lesion that is constantly trying to repair itself with new collagen formation and other tissue components. The single factor preventing repair of the lesion (periodontal pocket) is the never ending presence and persistence of the microbial insult on the tissues. This bacterial insult constantly and chronically stimulates immune and inflammatory cells causing degeneration of any newly formed tissue, along with further degrading existing healthy tissue. As the collagenous tissues imbedded in the root surface of the tooth (cementum) are destroyed, the pathogenic bacteria can invade the actual root surface of the tooth, as far as the cementodentinal junction, and may also enter the dentinal tubules. As the periodontal pocket migrates apically, bone loss becomes apparent. The loss of the bony architecture around a periodontal pocket is also an inflammatory, proliferative and degenerative process.
Bone loss and destruction apical to the periodontal pocket is a direct consequence of the bacterial penetration into and the inflammation associated with the base of the pocket. The change and more aggressive nature of the disease from a periodontal pocket to periodontitis with bony destruction occurs with a shift in the composition of the bacterial plaque in the area. As bony destruction begins, this shift is seen as a higher presence of motile and spirochete bacteria and a lesser presence of coccoid and straight rods. These motile bacteria further invade or bore into the supporting structures (collagen and bone) causing deeper immune and inflammatory responses- Once this bacterially fueled inflammatory process reaches the bone surrounding the periodontal ligament, bony destroying cells (osteoclasts) and white blood cells increase in number in the area, and bony destruction begins.
Conventional Periodontal Pocket Treatment
To successfully treat the periodontal pocket and periodontal disease, the local inflammation and the cause of the local inflammation must be eliminated. Once the cause of the inflammatory response is eliminated, a healthy individual will show remarkable capacity to heal his/her own periodontal tissues. With this statement as a universal given in the etiology of periodontal disease, the removal of the offending periodontal plaque and all of the inflammatory components that come with it is the primary focus of successful periodontal therapy. If this can be accomplished with minimal tissue manipulation (flap surgery only if absolutely necessary), keeping the area free of foreign bodies (removing calculus and not introducing time released solid or gelatinous drug delivery systems), and the almost complete removal of the offending microorganisms associated with plaque, healing will be improved and profound. This profound healing can be seen with new collagenous and epithelial attachments known as new periodontal ligament attachment. These occur only in areas not previously exposed to the pocket, and long junctional epithelium (a strong epithelial adaptation to the root surface) occurs in areas that were exposed to the pocket. Periodontal medicine has traditionally employed a variety of armamentarium and instrumentarium to accomplish this goal. Periodontal instruments have been invented and designed over the years for the specific goal of calculus removal, root planing and debridement, and removal of diseased periodontal tissues. In particular, periodontal scaling, root planing and curettage instruments are the armamentarium of choice to remove dental plaque, calculus, diseased cementum, and diseased pocket soft tissues. Below is a list of the most commonly employed names and uses of such armamentaria:
1) Sickle scalers to remove supragingival plaque and calculus: These have a flat surface with two cutting edges that converge at a cutting tip.
2) Curettes (Gracey curettes/scalers are most prevalent) for subgingival scaling, root planing, and soft tissue debridement: These have cutting edges that are set at a 90 degree angle to the lower end of the shank and come in a variety of shapes and sizes.
3) Hoe, chisel and file scalers to further aid in calculus and diseased cementum removal.
4) Ultrasonic instruments: These vibrate at from 20,000 to 45,000 hz in an effort to aid in the removal of calculus, deposits and plaque removal. Many ultrasonic instruments also pump water or local antimicrobials into the area to act as a flushing mechanism. Studies comparing ultrasonic and hand instrumentation used for periodontal scaling showed no significant statistical difference in probing depth reduction, bleeding on probing, and subgingival microflora reduction. Both hand instrumentation and ultrasonic scalers appear to have equal efficacy and treatment outcome. Also, as the etiology of periodontal disease has become more clear (ie. that it is bacterially driven), a number of pharmacological interventions have recently been tested and adapted as an adjunct to traditional mechanical treatment These pharmacological agents take the form of time released antimicrobial agents delivered into the periodontal pocket after mechanical debridement, to help eradicate pathogenic bacteria and hence decrease the tissues inflammatory response. However, they have significant limitations.
1) They must be sure to reach the intended site of action (a deep 3-dimensional periodontal pocket).
2) They must remain at an adequate concentration to be effective.
3) They must last for a sufficient duration of time to be effective.
To remain at an adequate concentration and last for a sufficient duration of time, there is a necessity for the intrasulcular delivery system of the antimicrobials to fill the physical space of the periodontal pocket with resorbable gels, resorbable spheres, impregnated chips for the duration of the therapy or drug delivery (usually 7 to 10 days). This in and of itself will be a foreign body preventing the immediate healing process and progress of long junctional epithelium formation at the tooth pocket interface after mechanical debridement. Also, the majority of local antimicrobials used are bacteriostatic in nature and never fully eliminate periodontal pathogens from the treatment site. This can only lead to long term resistant strains forming in the periodontal pocket in response to the sublethal effect of the antimicrobial.